title: Coagulation abnormalities in lacunar and cortical ischemic stroke are quite different.
abstract: In order to clarify the coagulation profile accompanying ischemic stroke, which may have implications on therapeutic strategies, we performed a prospective study to evaluate the hemostatic parameters in the first 24 h after the onset of cortical atherothrombotic infarct and lacunar infarction. Twenty-seven patients with cortical atherothrombotic infarction and 27 patients with lacunar infarction, diagnosed on clinical and CT-scan criteria, had blood samples taken within the first 24 h after onset of the stroke, and before anticoagulant treatment had been started. Levels of fibrinogen, von Willebrand factor, D-dimers, prothrombin factors 1 + 2, anti-thrombin III, and C-protein and S-proteins, were measured. Laboratory tests detected the following abnormalities: a protein C deficiency was observed in 1 case of cortical infarction and in 1 case of lacunar infarction; a decrease in S-protein was observed in 1 case of cortical infarction, and the presence of lupus anticoagulant in 4 cases (2 in cortical and 2 in lacunar infarction). Various degrees of coagulation activation were observed. Statistically significant activation of the coagulation was observed in the patients with cortical infarction, compared to normal patients adjusted for age: the levels of DDI were significantly raised (2298 +/- 2221 ng ml-1 vs. 750 +/- 400 ng ml-1) (p < 0.03) as were F1 + 2 levels (3.9 +/- 2.8 nmol l-1 vs. 1.5 +/- 0.9 nmol l-1). (p < 0.01). In the lacunar infarction group, there was a significant rise in F1 + 2 compared with normal patients adjusted for age (2.2 +/- 1.7 nmol l-1 vs. 1.5 +/- 0.9 nmol l-1) (p < 0.01), while the DDI level was in the normal range, when age was taken into account. In the cortical infarction group, we observed a significantly raised fibrinogen level (4.8 +/- 1.7 g l-1 vs. 3.7 +/- 1.0 g l-1) (p < 0.05) and von Willebrand factor level (271 +/- 104% vs. 178 +/- 103%) (p < 0.01) compared to the lacunar infarction group. In addition, we observed a significantly low level of S-protein in the cortical infarction group (105 +/- 29%) compared to the lacunar infarction group (127 +/- 28%) (p < 0.01). Confirmation of the role of enhanced thrombin activity in the pathogenesis of acute stroke may be an important determinant in its therapeutic management.
authors.affiliation: Neurology Department, CHU, Dijon, France.
authors.forename: M
authors.initials: M
authors.lastname: Giroud
authors.forename: F
authors.initials: F
authors.lastname: Dutrillaux
authors.forename: M
authors.initials: M
authors.lastname: Lemesle
authors.forename: F
authors.initials: F
authors.lastname: Volot
authors.forename: J L
authors.initials: JL
authors.lastname: Lorenzini
authors.forename: F
authors.initials: F
authors.lastname: Becker
authors.forename: R
authors.initials: R
authors.lastname: Dumas
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001780:Blood Coagulation Tests; D002545:Brain Ischemia / Q000209:etiology*; D002544:Cerebral Infarction / Q000209:etiology*; D002561:Cerebrovascular Disorders / Q000145:classification / Q000209:etiology*; D015161:Dementia, Multi-Infarct / Q000209:etiology*; D005260:Female; D006487:Hemostasis; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D013927:Thrombosis / Q000150:complications*